209 results match your criteria tafia inhibitor


S62798, a potent TAFIa inhibitor, accelerates endogenous fibrinolysis in a murine model of pulmonary thromboembolism.

Thromb Res 2021 08 11;204:81-87. Epub 2021 Jun 11.

Cardiovascular and Metabolic Diseases Research, Institut de Recherches Servier, Suresnes, France.

Enhancement of fibrinolysis constitutes a promising approach to treat thrombotic diseases. Venous thrombosis and thromboembolism risks are associated with increased plasma levels of TAFI (Thrombin Activatable Fibrinolysis Inhibitor) as well as its active form TAFIa. A new TAFIa inhibitor, namely S62798 has been identified. Read More

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Effect of Statin Therapy on the Carboxypeptidase U (CPU, TAFIa, CPB2) System in Patients With Hyperlipidemia: A Proof-of-concept Observational Study.

Clin Ther 2021 05 25;43(5):908-916. Epub 2021 Apr 25.

Laboratory of Medical Biochemistry, Department of Pharmaceutical Sciences, University of Antwerp, Antwerp, Belgium. Electronic address:

Purpose: Statins are commonly used in patients with hypercholesterolemia to lower their cholesterol levels and to reduce their cardiovascular risk. There is also considerable evidence that statins possess a range of cholesterol-independent effects, including profibrinolytic properties. This pilot study aimed to explore the influence of statins on procarboxypeptidase U (proCPU) biology and to search for possible effects and associations that can be followed up in a larger study. Read More

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Phosphinanes and Azaphosphinanes as Potent and Selective Inhibitors of Activated Thrombin-Activatable Fibrinolysis Inhibitor (TAFIa).

J Med Chem 2021 04 25;64(7):3897-3910. Epub 2021 Mar 25.

Institut de Recherches Servier, 11 rue des Moulineaux, 92150 Suresnes, et 125 Chemin de Ronde, 78290 Croissy-sur-Seine, France.

Selective and potent inhibitors of activated thrombin activatable fibrinolysis inhibitor (TAFIa) have the potential to increase endogenous and therapeutic fibrinolysis and to behave like profibrinolytic agents without the risk of major hemorrhage, since they do not interfere either with platelet activation or with coagulation during blood hemostasis. Therefore, TAFIa inhibitors could be used in at-risk patients for the treatment, prevention, and secondary prevention of stroke, venous thrombosis, and pulmonary embolisms. In this paper, we describe the design, the structure-activity relationship (SAR), and the synthesis of novel, potent, and selective phosphinanes and azaphosphinanes as TAFIa inhibitors. Read More

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Prolongation of clot lysis time by a direct thrombin inhibitor melagatran mediated by paradoxical enhancement of thrombin generation: comparison with a direct factor Xa inhibitor edoxaban.

Blood Coagul Fibrinolysis 2021 Apr;32(3):209-215

Biological Research Laboratories, R & D Division, Daiichi Sankyo Co., Ltd, Tokyo, Japan.

Previously, we reported that a direct thrombin inhibitor melagatran paradoxically increased thrombin generation in human plasma in the presence of thrombomodulin. The aim of this study is to test the hypothesis that melagatran may exert a deleterious effect on tissue-type plasminogen activator (t-PA)-induced fibrinolysis via enhancement of thrombin generation and subsequent activation of thrombin-activatable fibrinolysis inhibitor (TAFI) and factor XIII (FXIII). Clot formation in human plasma containing t-PA and thrombomodulin was induced by tissue factor. Read More

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Carboxypeptidase U (CPU, TAFIa, CPB2) in Thromboembolic Disease: What Do We Know Three Decades after Its Discovery?

Int J Mol Sci 2021 Jan 17;22(2). Epub 2021 Jan 17.

Laboratory of Medical Biochemistry, Department of Pharmaceutical Sciences, University of Antwerp, 2610 Wilrijk, Belgium.

Procarboxypeptidase U (proCPU, TAFI, proCPB2) is a basic carboxypeptidase zymogen that is converted by thrombin(-thrombomodulin) or plasmin into the active carboxypeptidase U (CPU, TAFIa, CPB2), a potent attenuator of fibrinolysis. As CPU forms a molecular link between coagulation and fibrinolysis, the development of CPU inhibitors as profibrinolytic agents constitutes an attractive new concept to improve endogenous fibrinolysis or to increase the efficacy of thrombolytic therapy in thromboembolic diseases. Furthermore, extensive research has been conducted on the in vivo role of CPU in (the acute phase of) thromboembolic disease, as well as on the hypothesis that high proCPU levels and the Thr/Ile325 polymorphism may cause a thrombotic predisposition. Read More

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January 2021

Characterisation of a novel thrombomodulin c.1487delC,p.(Pro496Argfs*10) variant and evaluation of therapeutic strategies to manage the rare bleeding phenotype.

Thromb Res 2021 01 9;197:100-108. Epub 2020 Nov 9.

Radcliffe Department of Medicine, University of Oxford, Oxford, UK; Oxford Haemophilia & Thrombosis Centre, NIHR Oxford Biomedical Research Centre, Oxford University Hospitals NHS Foundation Trust, Oxford, UK.

Introduction: A novel variant in the thrombomodulin (TM) gene, c.1487delC,p.(Pro496Argfs*10), referred to as Pro496Argfs*10, was identified in a family with an unexplained bleeding disorder. Read More

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January 2021

Selective inhibition of carboxypeptidase U may reduce microvascular thrombosis in rat experimental stroke.

J Thromb Haemost 2020 12 1;18(12):3325-3335. Epub 2020 Oct 1.

Laboratory for Vascular Translational Sciences, UMR_S1148 Inserm, University of Paris, Paris, France.

Background: Carboxypeptidase U (CPU, CPB2, TAFIa) is a potent attenuator of fibrinolysis. The inhibition of CPU is thus an interesting strategy for improving thrombolysis.

Objectives: The time course of CPU generation and proCPU consumption were assessed in an experimental rat model of acute ischemic stroke (AIS). Read More

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December 2020

Is there thrombin-activatable fibrinolysis inhibitor in saliva?

Br J Oral Maxillofac Surg 2020 11 4;58(9):e33-e37. Epub 2020 Jun 4.

Dept. of Dental Medicine, Karolinska Institutet, Huddinge; Department of Oral and Maxillofacial Surgery, Eastmaninstitutet, Folktandvården Stockholm AB; Health Technology Assessment-Odontology (HTA-O), Faculty of Odontology, Malmö University, Malmö. Electronic address:

The purpose of this study was to identify thrombin-activatable fibrinolysis inhibitor (TAFI) in saliva and to investigate the correlation between TAFI levels in saliva and plasma. Subjects included were healthy adults without diseases or medication that could affect coagulation. Samples of stimulated saliva and blood samples were obtained from 33 subjects. Read More

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November 2020

Activated thrombin-activatable fibrinolysis inhibitor (TAFIa) attenuates fibrin-dependent plasmin generation on thrombin-activated platelets.

J Thromb Haemost 2020 09;18(9):2364-2376

Thrombosis and Atherosclerosis Research Institute, Hamilton, ON, Canada.

Background: Thrombin-activated platelets can promote fibrinolysis by binding plasminogen in a fibrinogen-dependent manner and enhancing its activation by tissue-type plasminogen activator (t-PA). Whether t-PA also binds to activated platelets and the mechanism for regulation of platelet-dependent fibrinolysis remain unknown.

Objectives: Determine the mechanism of plasminogen and t-PA binding on thrombin-activated platelets and its regulation by activated thrombin-activatable fibrinolysis inhibitor (TAFIa). Read More

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September 2020

Thrombin activatable fibrinolysis inhibitor pathway alterations correlate with bleeding phenotype in patients with severe hemophilia A.

J Thromb Haemost 2020 02 15;18(2):381-389. Epub 2019 Oct 15.

Dipartimento di Scienze Biomediche e Oncologia Umana, Università degli Studi di Bari Aldo Moro, Bari, Italy.

Background: Patients with severe hemophilia A display varied bleeding phenotypes despite similar factor VIII (FVIII) activity levels.

Objective: We investigated different thrombin activatable fibrinolysis inhibitor (TAFI)-related variables in patients with severe hemophilia A and their possible correlation with bleeding tendency.

Patients/methods: Sixty-one patients with severe hemophilia A (FVIII:C <1%], treated on demand, were included. Read More

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February 2020

Plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels in acromegaly patients in remission

Turk J Med Sci 2019 10 24;49(5):1381-1385. Epub 2019 Oct 24.

Department of Rheumatology, Faculty of Medicine, Kırıkkale University, Kırıkkale, Turkey

Background/aim: Acromegaly is associated with increased morbidity andmortality, mostly due to cardiovascular complications.Plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels are associated with coagulation/fibrinolysis and inflammation. Plasma TAFI may play a role in arterial thrombosis in cardiovascular diseases. Read More

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October 2019

Combined effect of a direct oral anticoagulant edoxaban and an inhibitor of activated thrombin-activatable fibrinolysis inhibitor on clot lysis.

J Thromb Thrombolysis 2020 Jan;49(1):94-99

End-Organ Disease Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan.

Fibrinolysis is regulated by the thrombin/thrombin-activatable fibrinolysis inhibitor (TAFI) system. Thus, anticoagulants and inhibitors of TAFI are expected to accelerate fibrinolysis. The combined effects of an anticoagulant and a TAFIa inhibitor on fibrinolysis remain unknown. Read More

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January 2020

First-in-Human Study to Assess the Safety, Pharmacokinetics, and Pharmacodynamics of an Oral Formulation of DS-1040, an Inhibitor of the Activated Form of Thrombin-Activatable Fibrinolysis Inhibitor, in Healthy Subjects.

J Clin Pharmacol 2019 12 27;59(12):1669-1677. Epub 2019 Jun 27.

Daiichi Sankyo, Inc, Basking Ridge, NJ, USA.

DS-1040, a low-molecular-weight imidazole derivative, inhibits the enzymatic activity of thrombin-activatable fibrinolysis inhibitor (TAFIa), enhancing endogenous tissue plasminogen activator-triggered fibrinolysis. This first-in-human, randomized, placebo-controlled, phase 1 study evaluated the safety, pharmacokinetics (PK), and pharmacodynamics (PD) of an oral formulation of DS-1040. Healthy adults (aged 20-45 years; N = 56) were randomized 3:1 to receive DS-1040 orally administered as single ascending doses (50, 100, 200, or 400 mg) or placebo, or DS-1040 multiple ascending doses (100 mg once daily, 200 mg once daily, or 150 mg twice daily) or placebo for 14 days. Read More

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December 2019

Carboxypeptidase U (CPU, carboxypeptidase B2, activated thrombin-activatable fibrinolysis inhibitor) inhibition stimulates the fibrinolytic rate in different in vitro models.

J Thromb Haemost 2018 10 30;16(10):2057-2069. Epub 2018 Aug 30.

Laboratory of Medical Biochemistry, Department of Pharmaceutical Sciences, University of Antwerp, Wilrijk, Belgium.

Essentials AZD9684 is a potent inhibitor of carboxypeptidase U (CPU, TAFIa, CPB2). The effect of AZD9684 on fibrinolysis was investigated in four in vitro systems. The CPU system also attenuates fibrinolysis in more advanced hemostatic systems. Read More

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October 2018

Fibrinolytic potential of DS-1040, a novel orally available inhibitor of activated thrombin-activatable fibrinolysis inhibitor (TAFIa).

Thromb Res 2018 08 9;168:96-101. Epub 2018 Jul 9.

Rare Disease & LCM Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan.

An activated thrombin-activatable fibrinolysis inhibitor (TAFIa) attenuates fibrinolysis by removing C-terminal lysine/arginine residues from partially degraded fibrin. We have identified a novel low-molecular-weight inhibitor of TAFIa, DS-1040, to be potentially useful for treating thrombotic diseases. In this study, we investigated its in vitro pharmacological profile and in vivo effects in animal models of microthrombosis and bleeding. Read More

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Structural basis for the selective inhibition of activated thrombin-activatable fibrinolysis inhibitor (TAFIa) by a selenium-containing inhibitor with chloro-aminopyridine as a basic group.

Bioorg Med Chem Lett 2018 07 23;28(13):2256-2260. Epub 2018 May 23.

Laboratory of Drug Design and Medicinal Chemistry, Showa Pharmaceutical University, 3-3165 Higashi-Tamagawagakuen, Machida, Tokyo 194-8543, Japan. Electronic address:

Activated thrombin-activatable fibrinolysis inhibitor (TAFIa) is a target molecule for treating thromboembolic disorders. We previously reported that design and synthesis of compound 1 containing a selenol group and chloloaminopyridine. Compound 1 showed high inhibitory activity towards TAFIa, with a high degree of selectivity for TAFIa over carboxypeptidase N (CPN). Read More

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Tissue-type plasminogen activator transgenic rats for evaluating inhibitors of the activated form of thrombin-activatable fibrinolysis inhibitor.

Blood Coagul Fibrinolysis 2018 Apr;29(3):314-321

Rare Disease & LCM Laboratories.

: No rodent models are currently available for evaluating inhibitors of the activated form of thrombin-activatable fibrinolysis inhibitor (TAFIa) without exogenous supplementation of tissue-type plasminogen activator (tPA). Characterization of tPA transgenic rats as a tool for the nonclinical evaluation of TAFIa inhibitors is the objective of the current study. tPA transgenic rats were subjected to rat models of tissue-factor-induced thromboembolism, FeCl3-induced deep vein thrombosis (DVT) and arterial thrombosis, and tail bleeding. Read More

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Thrombin-activatable fibrinolysis inhibitor in human abdominal aortic aneurysm disease.

J Thromb Haemost 2017 11 25;15(11):2218-2225. Epub 2017 Sep 25.

Thrombosis and Tissue Repair Group, Division of Cardiovascular and Diabetes Research, Leeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, Leeds, UK.

Essentials Patients with abdominal aortic aneurysms (AAA) develop dense clots that are resistant to lysis. This study explores the role of thrombin-activatable fibrinolysis inhibitor (TAFI) in human AAA. There is evidence of chronically increased TAFI activation in patients with AAA. Read More

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November 2017

Plasma carboxypeptidase U (CPU, CPB2, TAFIa) generation during in vitro clot lysis and its interplay between coagulation and fibrinolysis.

Thromb Haemost 2017 07 6;117(8):1498-1508. Epub 2017 Jul 6.

Prof. D. Hendriks, Laboratory of Medical Biochemistry, University of Antwerp, Universiteitsplein 1, B-2610 Wilrijk, Belgium, Tel.: +32 3 265 27 27, E-mail:

Carboxypeptidase U (CPU, CPB2, TAFIa) is a basic carboxypeptidase that is able to attenuate fibrinolysis. The inactive precursor procarboxypeptidase U is converted to its active form by thrombin, the thrombin-thrombomodulin complex or plasmin. The aim of this study was to investigate and characterise the time course of CPU generation in healthy individuals. Read More

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Thrombin activatable fibrinolysis inhibitor (TAFI) - A possible link between coagulation and complement activation in the antiphospholipid syndrome (APS).

Thromb Res 2017 Oct 24;158:168-173. Epub 2017 Jun 24.

Unit of Rheumatology, Department of Medicine, Solna, Karolinska Institutet, Karolinska University Hospital, SE-171 76 Stockholm, Sweden.

Background: Thrombosis and complement activation are pathogenic features of antiphospholipid syndrome (APS). Their molecular link is Plasma carboxypeptidase-B, also known as thrombin activatable fibrinolysis inhibitor (TAFIa), which plays a dual role: anti-fibrinolytic, by cleaving carboxyl-terminal lysine residues from partially degraded fibrin, and anti-inflammatory, by downregulating complement anaphylatoxins C3a and C5a.

Aim: To investigate the levels of TAFI (proenzyme) and TAFIa (active enzyme) in relation to complement activation, fibrin clot permeability and fibrinolytic function in clinical and immunological subsets of 52 APS patients and 15 controls. Read More

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October 2017

Activated TAFI Promotes the Development of Chronic Thromboembolic Pulmonary Hypertension: A Possible Novel Therapeutic Target.

Circ Res 2017 Apr 13;120(8):1246-1262. Epub 2017 Mar 13.

From the Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan (T.S., K. Satoh, N.Y., N.K., J.O., R.K., K.N., E.A.-M., M.A.H.S., S.S., M.N., K. Suzuki, S.M., H.S.); and Department of Hematology, Stanford School of Medicine, CA (J.M.).

Rationale: Pulmonary hypertension is a fatal disease; however, its pathogenesis still remains to be elucidated. Thrombin-activatable fibrinolysis inhibitor (TAFI) is synthesized by the liver and inhibits fibrinolysis. Plasma TAFI levels are significantly increased in chronic thromboembolic pulmonary hypertension (CTEPH) patients. Read More

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The impact of the endothelial protein C receptor on thrombin generation and clot lysis.

Thromb Res 2017 Apr 3;152:30-37. Epub 2017 Feb 3.

Department of Medicine at McMaster University, Hamilton, Ontario L8L 0A6, Canada; Thrombosis and Atherosclerosis Research Institute, Hamilton, Ontario L8L 0A6, Canada. Electronic address:

Introduction: When thrombin is bound to thrombomodulin (TM), it becomes a potent activator of protein C (PC) and thrombin-activable fibrinolysis inhibitor (TAFI). Activation of PC is enhanced when PC is bound to the endothelial protein C receptor (EPCR). Activated protein C (APC) inhibits thrombin generation while activated TAFI (TAFIa) attenuates fibrinolysis. Read More

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A first-in-human study of DS-1040, an inhibitor of the activated form of thrombin-activatable fibrinolysis inhibitor, in healthy subjects.

J Thromb Haemost 2017 05 11;15(5):961-971. Epub 2017 Mar 11.

Daiichi Sankyo Pharma Development, Edison, NJ, USA.

Essentials DS-1040 inhibits the activated form of thrombin-activatable fibrinolysis inhibitor (TAFIa). Infusion of DS-1040 was safe and well tolerated in healthy young and elderly subjects. DS-1040 substantially decreased TAFIa activity but had no impact on bleeding time. Read More

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Fibrinolysis inhibitors in plaque stability: a morphological association of PAI-1 and TAFI in advanced carotid plaque.

J Thromb Haemost 2017 04 28;15(4):758-769. Epub 2017 Feb 28.

CVMD Translational Medicine Unit, Early Clinical Development, AstraZeneca R&D Mölndal, Mölndal, Sweden.

Essentials Fibrinolysis inhibitors are localized in advanced atheroma by immunohistology of endarterectomies. Neovascular endothelium/neocapillaries show thrombin-activatable fibrinolysis inhibitor (TAFI). Macrophage areas show free plasminogen activator inhibitor (PAI-1), notably in the vulnerable part. Read More

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Activated thrombin-activatable fibrinolysis inhibitor attenuates the angiogenic potential of endothelial cells: potential relevance to the breast tumour microenvironment.

Clin Exp Metastasis 2017 02 25;34(2):155-169. Epub 2017 Jan 25.

Department of Biochemistry, Room 4245A Robarts Research Institute, University of Western Ontario, 1151 Richmond Street North, London, ON, N5B 3P7, Canada.

Thrombin-activatable fibrinolysis inhibitor (TAFI) is a basic carboxypeptidase zymogen present in blood plasma. Proteolytic activation of TAFI by thrombin, thrombin in complex with the endothelial cell cofactor thrombomodulin, or plasmin results in an enzyme (TAFIa) that removes carboxyl-terminal lysine residues from protein and peptide substrates, including cell-surface plasminogen receptors. TAFIa is therefore capable of inhibiting plasminogen activation in the pericellular milieu. Read More

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February 2017

Impaired plasma clot lysis and its determinants in patients with obstructive sleep apnea syndrome.

Blood Coagul Fibrinolysis 2016 Dec;27(8):892-898

aJohn Paul II Hospital bInstitute of Cardiology, Jagiellonian University Medical College, Krakow, Poland.

Evidence indicates that hypercoagulability and impaired fibrinolysis have been observed in patients with obstructive sleep apnea syndrome (OSAS). It is unclear which factors determine prolonged fibrin clot lysis in OSAS. One hundred and sixty-five consecutive patients suspected of OSAS underwent overnight polysomnography. Read More

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December 2016

Sulfamide as Zinc Binding Motif in Small Molecule Inhibitors of Activated Thrombin Activatable Fibrinolysis Inhibitor (TAFIa).

J Med Chem 2016 Oct 17;59(20):9567-9573. Epub 2016 Oct 17.

Sanofi R&D , Industriepark Höchst Building G838, D-65926 Frankfurt am Main, Germany.

Previously disclosed TAFIa inhibitors having a urea zinc-binding motif were used as the starting point for the development of a novel class of highly potent inhibitors having a sulfamide zinc-binding motif. High-resolution X-ray cocrystal structures were used to optimize the structures and reveal a highly unusual sulfamide configuration. A selected sulfamide was profiled in vitro and in vivo and displayed a promising ADMET profile. Read More

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October 2016

Isolation, Co-Crystallization and Structure-Based Characterization of Anabaenopeptins as Highly Potent Inhibitors of Activated Thrombin Activatable Fibrinolysis Inhibitor (TAFIa).

Sci Rep 2016 09 8;6:32958. Epub 2016 Sep 8.

Sanofi-Aventis Deutschland GmbH, Industriepark Höchst, 65926, Frankfurt am Main, Germany.

Mature thrombin activatable fibrinolysis inhibitor (TAFIa) is a carboxypeptidase that stabilizes fibrin clots by removing C-terminal arginines and lysines from partially degraded fibrin. Inhibition of TAFIa stimulates the degradation of fibrin clots and may help to prevent thrombosis. Applying a lead finding approach based on literature-mining, we discovered that anabaenopeptins, cyclic peptides produced by cyanobacteria, were potent inhibitors of TAFIa with IC50 values as low as 1. Read More

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September 2016

Stimulation of thrombin- and plasmin-mediated activation of thrombin-activatable fibrinolysis inhibitor by anionic molecules.

Thromb Res 2016 Oct 17;146:7-14. Epub 2016 Aug 17.

Department of Experimental Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; Department of Plasma Proteins, Sanquin Research, Amsterdam, The Netherlands.

Background: Thrombin-activatable fibrinolysis inhibitor (TAFI) is a proenzyme that, once activated, attenuates fibrinolysis by removing C-terminal lysine residues from partially degraded fibrin. TAFI can be activated by thrombin or plasmin via a cleavage at Arg92 that removes the activation peptide from the enzyme, TAFIa. Thrombomodulin enhances thrombin-mediated TAFI activation and glycosaminoglycans enhance plasmin-mediated TAFI activation. Read More

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October 2016

Changes in Activated Thrombin-Activatable Fibrinolysis Inhibitor Levels Following Thrombolytic Therapy in Ischemic Stroke Patients Correlate with Clinical Outcome.

Cerebrovasc Dis 2016 8;42(5-6):404-414. Epub 2016 Jul 8.

Laboratory Haemostasis, Inserm UMR 1062, Inra UMR 1260, Aix Marseille University, Marseille, France.

Background And Purpose: Thrombin-activatable fibrinolysis inhibitor (TAFI) activation following thrombolysis may affect thrombolysis effectiveness in acute ischemic stroke (AIS). To support this hypothesis, we propose to study the relationship between TAFI consumption, activated/inactivated TAFI (TAFIa/ai) and stroke severity and outcome in 2 groups of AIS patients, one treated and one untreated with intravenous recombinant tissue type plasminogen activator (rt-PA).

Methods: In this prospective, longitudinal, multicenter, observational study, we aimed to study the association between TAFIa/ai and stroke outcome. Read More

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December 2017